| Project/Area Number |
13854022
|
|---|
| Research Category |
Grant-in-Aid for Scientific Research (S)
|
| Allocation Type | Single-year Grants |
|---|
| Research Field |
病態科学系歯学(含放射線系歯学)
|
|---|
| Research Institution | The University of Tokyo (2002-2005)
Tokyo Medical and Dental University (2001) |
|---|
Principal Investigator |
ICHIJO Hidenori The University of Tokyo, Graduate School of Pharmaceutical Sciences, Professor, 大学院・薬学系研究科, 教授 (00242206)
|
|---|
| Co-Investigator(Kenkyū-buntansha) |
TAKEDA Kohsuke The University of Tokyo, Graduate School of Pharmaceutical Sciences, Associate Professor, 大学院・薬学系研究科, 助教授 (10313230)
MATSUZAWA Atsushi The University of Tokyo, Graduate School of Pharmaceutical Sciences, Research Associate, 大学院・薬学系研究科, 助手 (80345256)
NISHITOH Hideki Tokyo Medical and Dental University, Department of Oral Restitution, Graduate School, Center of Excellence Program for, Frontier Research on Molecular Destruction and Reconstruction of Tooth and Bone, Research Associate Professor, 大学院・医歯学総合研究科, COE拠点形成特任教員(研究員) (00332627)
|
|---|
| Project Period (FY) |
2001 – 2005
|
| Project Status |
Completed (Fiscal Year 2005)
|
| Budget Amount *help |
¥123,110,000 (Direct Cost: ¥94,700,000、Indirect Cost: ¥28,410,000)
Fiscal Year 2005: ¥24,700,000 (Direct Cost: ¥19,000,000、Indirect Cost: ¥5,700,000)
Fiscal Year 2004: ¥24,570,000 (Direct Cost: ¥18,900,000、Indirect Cost: ¥5,670,000)
Fiscal Year 2003: ¥24,700,000 (Direct Cost: ¥19,000,000、Indirect Cost: ¥5,700,000)
Fiscal Year 2002: ¥24,700,000 (Direct Cost: ¥19,000,000、Indirect Cost: ¥5,700,000)
Fiscal Year 2001: ¥24,440,000 (Direct Cost: ¥18,800,000、Indirect Cost: ¥5,640,000)
|
|---|
| Keywords | ASK1 / MAP Kinase / Apoptosis / Stress / Calcium / 自然免疫 / ASKファミリー / ASK2 |
|---|
| Research Abstract |
This research program aimed at disclosing the molecular mechanisms by which cells convert quantitative difference of signals into qualitative difference of responses. We investigated the stress responses with main focuses on the regulatory mechanisms of ASK family proteins by physico-chemical stresses. More concretely, following studies have been performed ; 1)oxidative stress- and endoplasmic reticulum stress-induced activation mechanisms of ASK1, 2)development of monitoring system of ASK1 activity, 3)search for small compounds which inhibit ASK1 activity, 4)activation mechanisms of ASK family proteins, 5)establishment of knockout mice of ASK family genes, 6)the effects of ASK1 gene deletion on the gene expression, protein modification and cell fate. Based on these experiments, we found that durations of activated proteins downstream of ASK1 play important roles in generation of qualitative differences of cellular responses. These excellent results suggested that the studies of stress responses through ASK family may lead to the development of revolutionary therapeutic drugs for neurodegenerative diseases and inflammation.
|
